Loneliness can make you sick
For older adults, perceived social isolation is a major health risk that can increase the risk of premature death by 14 percent.
A team of researchers, including UChicago psychologist and leading loneliness expert John Cacioppo, released a study shedding new light on how loneliness triggers physiological responses that can ultimately make us sick.
The paper, published in the Proceedings of the National Academy of Sciences, shows that loneliness leads to fight-or-flight stress signaling, which can ultimately affect the production of white blood cells.
For the study, the team examined gene expression in leukocytes, cells of the immune system that are involved in protecting the body against bacteria and viruses.
The leukocytes of lonely humans and macaques showed the effects of CTRA–an increased expression of genes involved in inflammation and a decreased expression of genes involved in antiviral responses. But the study also revealed several important new pieces of information about loneliness’ effect on the body.
First, the researchers found that loneliness predicted future CTRA gene expression measured a year or more later. Interestingly, CTRA gene expression also predicted loneliness measured a year or more later. Leukocyte gene expression and loneliness appear to have a reciprocal relationship, suggesting that each can help propagate the other over time. These results were specific to loneliness and could not be explained by depression, stress or social support.
Next, the team investigated the cellular processes linking social experience to CTRA gene expression in rhesus macaque monkeys at the California National Primate Research Center, which had been behaviorally classified as high in perceived social isolation. Like the lonely humans, the “lonely like” monkeys showed higher CTRA activity. They also showed higher levels of the fight-or-flight neurotransmitter, norepinephrine.
Finally, the researchers determined that this monocyte-related CTRA shift had real consequences for health. In a monkey model of viral infection, the impaired antiviral gene expression in “lonely like” monkeys allowed simian immunodeficiency virus (the monkey version of HIV) to grow faster in both blood and brain.
Taken together, these findings support a mechanistic model in which loneliness results in fight-or-flight stress signaling, which increases the production of immature monocytes, leading to up-regulation of inflammatory genes and impaired anti-viral responses. The “danger signals” activated in the brain by loneliness ultimately affect the production of white blood cells. The resulting shift in monocyte output may both propagate loneliness and contribute to its associated health risks.
Category: Features, Health alert
